Asian Cardiovasc Thorac Ann 2004;12:296-299
© 2004 Asia Publishing EXchange Ltd
Surgical Closure of Atrial Septal Defect in Children Under Two Years of Age
Usha Parvathy, MCh,
Komarakshi R Balakrishnan, MCh,
Madathil S Ranjith, MD1,
Richard Saldanha, MCh,
Mahesh Vakamudi, MD2
Department of Cardiothoracic Surgery
1 Department of Cardiology
2 Department of Cardiac Anaesthesia, Sri Ramachandra Medical College University Hospital, Chennai, India
For reprint information contact: Usha Parvathy, MCh Tel: 91 44 2476 8403 Fax: 91 44 2476 7008 Email: cvskrb{at}giasmd01.vsnl.net.in Department of Cardiothoracic Surgery, Sri Ramachandra Medical College University Hospital, Porur, Chennai 600116, India.
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ABSTRACT
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Infants with atrial septal defects are seldom symptomatic and usually require elective surgery between 2 and 4 years of age. However a small minority is symptomatic and management at this age has been controversial. This study evaluated surgical closure of atrial septal defect below 2 years of age. Eighteen infants with a mean age of 13.4 ± 5.7 months were operated on for secundum atrial septal defect from 1994 to 2001. Fourteen patients were symptomatic with failure to thrive in 7 and recurrent respiratory infections in 7, one had increasing cardiomegaly, and 3 were operated on early for social reasons. The defect was isolated in 11 patients (61%) and the other 7 (39%) had minor associated lesions requiring additional procedures such as ductal ligation, direct closure of a tiny ventricular septal defect, and inspection of the mitral valve. There were no early or late deaths. The postoperative course was complicated by pulmonary problems in 4 cases. Of the 16 patients available for follow-up, 14 were asymptomatic and 2 were symptomatically improved. Most showed a dramatic improvement in growth and development. These gratifying results indicate that consideration should be given to early surgical closure of atrial septal defect in symptomatic infants.
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INTRODUCTION
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The natural history of secundum atrial septal defect (ASD) in infancy and early childhood is usually benign, with surgery being performed electively between 2 and 4 years of age. Occasionally, symptomatic infants with ASD are encountered; warranting early surgical closure.1 Device closure presents technical difficulties in small infants. We report our experience with 18 children less than 2 years of age who underwent surgical closure of secundum ASD for various indications over a period of 7 years.
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PATIENTS AND METHODS
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Eighteen (10%) of the 180 consecutive patients with ASD surgically corrected in our institute from September 1994 to September 2001 were under 2 years of age (mean age, 13.4 ± 5.7 months; median, 12.0 months). Nine were under 1 year old and the other 9 were between 1 and 2 years old; 2 were less than 6 months old. Weights ranged from 5.2 to 12 kg (mean, 7.5 kg ± 2.2; median, 7.0 kg). There were 10 males and 8 females, 14 were symptomatic with failure to thrive in 7 and recurrent respiratory tract infections requiring frequent hospitalization in 7; 6 (33%) were in congestive heart failure and on digoxin and diuretic therapy. All had cardiomegaly and pulmonary plethora on chest radiography, with a cardiothoracic ratio between 0.6 and 0.7 in 15 cases, and 0.7 to 0.8 in 3 cases. Echocardiography showed an isolated ASD in 11 infants and minor associated lesions in 7 (Table 1
). Pulmonary artery hypertension assessed by echocardiography was moderate in 6, severe (but sub-systemic) in 2, and mild in the rest. Cardiac catheterization was not performed in any of the patients. Two children had been operated on previously for extracardiac anomalies (hypospadias and pelvic-ureteric junction anomaly). There was facial dysmorphism in one infant and Down’s syndrome in another. The indications for surgery were failure to thrive in 7 infants, recurrent respiratory infections in 7, one was mildly symptomatic but showed an increasing cardiothoracic ratio, and the other 3 underwent early surgery for social reasons: parental preference for early surgery in 2 cases; and in an orphan, early surgery was decided prior to adoption.
Surgery was performed under moderate hypothermia in all cases, with cardioplegic arrest in 14 and fibrillatory arrest in 4. The aortic crossclamp time varied from 3 to 17 minutes (mean, 9.1 ± 5.6 min; median, 8.50 min), and the cardiopulmonary bypass time was 34 to 54 minutes (mean, 29.5 ± 11.1 min; median, 28.0 min). Surgical details are given in Table 2. All patients had right atrial and right ventricular dilatation. The size of the ASD was usually 1.5 2.5 cm, and one symptomatic child had a 5 mm ASD. Direct closure of the ASD was carried out in 11 patients and the other 7 required a pericardial patch; one patient with severe pulmonary artery hypertension and an abnormal mitral valve had a fenestrated ASD patch. One patient had an additional tiny muscular ventricular septal defect that was closed directly. The mitral valve was inspected in 4 patients suspected to have mitral valve anomalies. In one of these, membrane forming a partial Cor triatriatum had to be excised, 2 had mild mitral stenosis, and one had a fairly normal mitral valve. In all 4 patients, the orifice was found to be adequate and the valve was competent.
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RESULTS
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All infants survived the surgery. One child with a small ductus and right pulmonary artery stenosis had difficulty in weaning from bypass due to pulmonary hypertensive crisis. Four children (2 with a mild mitral valve abnormality, 1 with right pulmonary artery stenosis, and 1 with isolated ASD) required inotropic support due to pulmonary hypertension in 2 and mild myocardial dysfunction in 2. The inotropics were discontinued after 2 days in 3 patients, and at 6 days in one whose postoperative period was complicated. The duration of ventilation ranged from 4 to 216 hours (mean, 25.99 hours; median, 15 hours). One girl with ASD, mild mitral stenosis, and severe pulmonary artery hypertension had a stormy postoperative course with difficulty in weaning from the ventilator due to wet lungs and a high partial pressure of CO2 in the blood. She needed reintubation on the 4th postoperative day, and was detected to have ventricular dysfunction and a very small mid-muscular ventricular septal defect on echocardiography. Ventilatory and inotropic support was needed for 6 days and 8 days, respectively. Thereafter, she recovered well. Three other children had collapse with consolidation of lung, which settled with antibiotics and chest physiotherapy. One child with isolated ASD had a persistent low oxygen saturation of 82% on room air, which increased to only 90% on oxygen.
Contrast echocardiographic studies were negative for intracardiac shunts. Her O2 saturation improved gradually over the next 3 days. She was detected to have a pulmonary arteriovenous fistula later at follow-up.
Postoperatively, the majority of patients were in sinus rhythm, 5 were in junctional rhythm that reverted to sinus rhythm after transient pacing, and 2 had first-degree heart block needing atrial pacing for 2 3 days. Intensive care unit stay was 1.5 to 17.5 days (mean, 4 ± 3.6 days; median, 3.0 days), and hospital stay was 4 to 25 days (mean, 8.7 ± 5.2 days; median, 7.5 days). The follow-up ranged from 3 months to 5 years (mean, 9 months). All patients were symptomatically better and doing well with regard to growth and development. Fourteen were asymptomatic, 2 were symptomatically better and developmentally much improved, and 2 were lost to follow-up. Chest radiography showed a marked reduction in cardiomegaly in all cases. Those with a cardiothoracic ratio of 0.8 showed a reduction to 0.6 or less. Follow-up echocardiography showed no residual defects except in the child who had a fenestrated patch. The small muscular ventricular septal defect closed within 9 months. Among the patients with mitral valve anomalies, echocardiography showed trivial mitral stenosis in 2, mild stenosis in 1, and a normal orifice in 1.
The child detected to have a pulmonary arteriovenous fistula continued to be symptomatic for the first 6 months after which she showed improvement in symptoms, growth, and development. Among the children with moderate or severe pulmonary hypertension, one had mild residual pulmonary hypertension, and pulmonary pressures normalized in the others. The child with right pulmonary artery stenosis had a very mild gradient of 20 mm Hg on echocardiography. Weight gain and development were good in all except one child with a mitral valve anomaly and another with dysmorphism who still lags behind despite being symptomatically better with improved physical development, probably due to a chromosomal abnormality.
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DISCUSSION
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Although ASD is one of the most frequently encountered congenital malformations of the heart, it is not commonly operated on in infancy. For the vast majority of patients, the natural history of the defect is characterized by a relatively benign course, and rarely does it cause problems in early life.1 The incidence of symptomatic ASD in infancy varies from 5% as reported by Dimich and colleagues2 to 10% 13.7%; symptomatic ASD requiring surgery is even rarer (3.7%) at that age.3,4 Elective surgery is usually planned at 2 4 years of age. Although many of these defects can be closed safely at 6 12 months of age, in asymptomatic children, the trend is to close the ASD at 2 4 years old before the child goes to school. In the absence of health insurance in our country, this gives parents more time to arrange finance for the surgery.
While a high incidence of spontaneous closure of ASD in neonates and infants has been reported, others claim that these are only flap-incompetent foramen ovale.5 These patients are managed medically, allowing sufficient time for spontaneous closure to be observed.5,6 A few reports mention that ASD may cause congestive heart failure in infancy.3,7,8 The possible explanations for congestive failure in infants include a larger than normal left-to-right shunt, the presence of another large left-to-right shunt, left-sided obstructive lesions, earlier than usual decreases in pulmonary vascular resistance, abnormal ventricular compliance, and abnormal atrial compliance.3 Congestive failure can be expected to improve with conservative treatment.8,10 Spontaneous closure of ASD in cardiac failure and after infancy has been reported.10
It is postulated that early vasodilatation of the pulmonary vascular bed could be the origin of a left-to-right shunt in patients with no increase in pulmonary vascular resistance.11 Bull and colleagues12 hypothesized that pulmonary vascular obstructive disease is the primary abnormality in symptomatic infants, ASD being an incidental although exacerbating finding, as more than half of the symptomatic children in their series had pulmonary hypertension at cardiac catheterization. Two other reports state similar findings.13,14 Children with ASD have a lower respiratory compliance than normal cohorts.15 In evaluating the implications for anesthetic management, Shulman and colleagues15 found that although respiratory compliance was lower during sedation, it was not lower during anesthesia and cardiopulmonary bypass in infants and children with ASD, compared to controls undergoing non-thoracic surgery. No direct relationship has been established between the degree of left-to-right shunting and the onset of congestive heart failure. It is thought that certain infants have impaired myocardial function and cannot tolerate the volume overload caused by a left-to-right shunt.16 Thus, this usually benign lesion may produce intractable congestive failure and death in infancy.17 The prognosis for infants and young children who present with intractable congestive failure, often complicated by pneumonia and failure to thrive, is extremely poor.17 This subset of patients benefit most from early surgery.1,16 There are very few reports on the surgical closure of ASD in infancy. Significant mortality was noted by Hunt and Lucas3 in their series where both patients operated on in the first year of life died. Two of 6 infants in the series of Bull and colleagues12 died, and 2 had a protracted postoperative course due to pulmonary vascular disease. However, there are some recent reports where improved techniques have shown favorable results of early operative intervention for symptomatic secundum ASD.4,13,14,18,19
In our series of 18 patients, only 3 were asymptomatic. All had clinical and radiological evidence of a large left-to-right shunt, and echocardiography provided a clear diagnosis. Due to the cost of devices in our country, and the technical difficulties in small infants, surgery was preferred. Although the crossclamp and cardiopulmonary bypass times are short, it is safer to use moderate hypothermia in small infants for better protection and to allow for any unexpected problems. Direct closure was performed when the edges could be approximated; a pericardial patch was used in cases of a large ASD and in infants with mild mitral valve anomalies. The experience of Mainwaring and colleagues13 with 6 infants who underwent surgical closure of isolated secundum ASD, suggests that failure to thrive associated with this lesion has a noncardiac basis as 5 patients demonstrated little or no improvement in feeding or growth rate following surgery. The operation was performed on the premise that elimination of volume overload results in symptomatic improvement. A similar experience was earlier reported by Bull and colleagues.12 On the other hand, Navajas and colleagues19 found that none of their 7 infants with secundum ASD responded to medical treatment, and the 5 who were operated on showed significant clinical improvement with normal growth and weight curves at follow-up, thus emphasizing the importance of early surgery. In our series, most patients showed a growth and developmental spurt after surgery, except one with an abnormal mitral valve and another with dysmorphism. These gratifying early and long-term results indicate that consideration should be given to early surgical closure of ASD in those patients who are symptomatic and do not respond promptly and completely to medical therapy.
Presented as a poster at the 3rd Annual Conference of the Pediatric Cardiac Society of India, Chennai, India, January 20 22, 2001.
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ABSTRACT
INTRODUCTION
